Various strains of Chlamydia psittaci and C. trachomatis will be grown in L cells, HeLa cells, and mouse peritoneal macrophages. The following questions will be asked: 1. What is the chemical nature and the biological specificity of the trypsin-labile sites on the L cell and the heat-sensitive sites on C. psittaci that are responsible for rapid ingestion of the parasite? 2. Can similar recognition sites be demonstrated on other host cells and on other chlamydial cells? 3. What is the mechanism of host-cell killing by low and moderate multiplicities of C. psittaci? It is the same or different from the already demonstrated lethality of high chlamydial multiplicities? 4. What are the mechanisms whereby C. psittaci and C. trachomatis injure and kill mouse peritoneal macrophages? Is it the same as for non-professional phagocytes such as L cells?